Experimental Models of High Fat Obesity and Leucine Supplementation

2015 ◽  
pp. 219-227
Author(s):  
Yuran Xie ◽  
Zhonglin Xie
Keyword(s):  
Experimental Models ◽  
High Fat ◽  
Leucine Supplementation

Abstract 156: Involvement of β-adrenergic System in Myocardial Dysfunction Induced by Obesity

2014 ◽  
Vol 115 (suppl_1) ◽  
Author(s):  
Ana Paula Lima-Leopoldo ◽  
Artur Ferron ◽  
Bruno Jacobsen ◽  
Dijon Campos ◽  
Renata Luvizotto ◽  
...  
Keyword(s):  
Myocardial Dysfunction ◽  
Myocardial Contraction ◽  
Experimental Models ◽  
The Body ◽  
Adrenergic System ◽  
Standard Diet ◽  
Adrenergic Stimulation ◽  
High Fat ◽  
Functional Changes ◽  
Adiposity Index

Several structural and functional changes of the heart have often been associated with human and experimental models of obesity. Some factors have been suggested as responsible for possible cardiac abnormalities in models of obesity, among them β-adrenergic system, an important mechanism of regulation of myocardial contraction and relaxation. The objetive of present study was to evaluate the . Thirty-day-old male Wistar rats were assigned to one of two groups: control (C) and obese (Ob). The C group was fed a standard diet and Ob group was fed cycles of four unsaturated high-fat diets for 15 weeks. The body fat was measured from the sum of the individual fat pad weights and the obesity was defined by adiposity index. Isolated papillary muscle preparation was performed under basal conditions and after inotropic and lusitropic maneuvers. β-adrenergic system was evaluated by using cumulative concentrations of isoproterenol and Western Blot. After 15 weeks, the Ob rats developed higher adiposity index than C rats. Obesity promoted comorbities such as glucose intolerance, insulin resistance, hyperleptinemia, and dyslipidemia; however, were not associated with changes in systolic blood pressure. The cardiac structure results post-death showed that obesity caused cardiac hypertrophy. Furthermore, Ob muscles developed similar baseline data, but myocardial responsiveness to post-rest contraction stimulus and increased extracellular Ca2+ was compromised. There were no changes in cardiac function between groups after β-adrenergic stimulation. The obesity was not accompanied by changes in protein expression of Gsα, β1 and β2 adrenergic receptors. In conclusion, the myorcardial dysfunction caused by unsaturated high-fat diet-induced obesity, after 15 weeks, is not related to β-adrenergic system impairment.

Clerodendron glandulosum.Coleb extract ameliorates high fat diet/fatty acid induced lipotoxicity in experimental models of non-alcoholic steatohepatitis

2010 ◽  
Vol 48 (12) ◽  
pp. 3424-3431 ◽  
Author(s):  
Ravirajsinh N. Jadeja ◽  
Menaka C. Thounaojam ◽  
Deven S. Dandekar ◽  
Ranjitsinh V. Devkar ◽  
A.V. Ramachandran
Keyword(s):  
Fatty Acid ◽  
High Fat Diet ◽  
Experimental Models ◽  
High Fat ◽  
Alcoholic Steatohepatitis

scholarly journals Diet-Induced Rabbit Models for the Study of Metabolic Syndrome

Animals ◽  
2019 ◽  
Vol 9 (7) ◽  
pp. 463 ◽  
Author(s):  
Wilson M. Lozano ◽  
Oscar J. Arias-Mutis ◽  
Conrado J. Calvo ◽  
Francisco J. Chorro ◽  
Manuel Zarzoso
Keyword(s):  
Metabolic Syndrome ◽  
Ldl Cholesterol ◽  
Low Density Lipoprotein ◽  
Caloric Intake ◽  
Density Lipoprotein ◽  
Experimental Models ◽  
Processed Food ◽  
High Fat ◽  
Hypertension Diagnosis ◽  
Transgenic Strains

Obesity and metabolic syndrome (MetS) have become a growing problem for public health and clinical practice, given their increased prevalence due to the rise of sedentary lifestyles and excessive caloric intake from processed food rich in fat and sugar. There are several definitions of MetS, but most of them describe it as a cluster of cardiovascular and metabolic alterations such as abdominal obesity, reduced high-density lipoprotein (HDL) and elevated low-density lipoprotein (LDL) cholesterol, elevated triglycerides, glucose intolerance, and hypertension. Diagnosis requires three out of these five criteria to be present. Despite the increasing prevalence of MetS, the understanding of its pathophysiology and relationship with disease is still limited. Indeed, the pathological consequences of MetS components have been reported individually, but investigations that have studied the effect of the combination of MeS components on organ pathological remodeling are almost nonexistent. On the other hand, animal models are a powerful tool in understanding the mechanisms that underlie pathological processes such as MetS. In the first part of the review, we will briefly overview the advantages, disadvantages and pathological manifestations of MetS in porcine, canine, rodent, and rabbit diet-induced experimental models. Then, we will focus on the different dietary regimes that have been used in rabbits to induce MetS by means of high-fat, cholesterol, sucrose or fructose-enriched diets and their effects on physiological systems and organ remodeling. Finally, we will discuss the use of dietary regimes in different transgenic strains and special rabbit breeds.

scholarly journals High-fat diet-induced glucose dysregulation is independent of changes in islet ACE2 in mice

2016 ◽  
Vol 311 (6) ◽  
pp. R1223-R1233 ◽  
Author(s):  
Harshita Chodavarapu ◽  
Kavaljit H. Chhabra ◽  
Huijing Xia ◽  
Vinayak Shenoy ◽  
Xinping Yue ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Glucose Homeostasis ◽  
High Fat Diet ◽  
Cell Function ◽  
Physiological Role ◽  
Experimental Models ◽  
Minor Role ◽  
Ang Ii ◽  
High Fat

While restoration of ACE2 activity in the pancreas leads to improvement of glycemia in experimental models of Type 2 diabetes, global deficiency in ACE2 disrupts β-cell function and impairs glucose tolerance in mice, demonstrating the physiological role of ACE2 in glucose homeostasis. Although the contribution of pancreatic ACE2 to glucose regulation has been demonstrated in genetic models of diabetes and in models with overexpression of the renin-angiotensin system (RAS), it is unclear whether islet ACE2 is involved in glycemic control in common models of human Type 2 diabetes. To determine whether diet-induced diabetes deregulates glucose homeostasis via reduction of ACE2 in the pancreatic islets, wild-type (WT) and ACE2 knockout (KO) male mice were fed a high-fat diet (HFD) for 16 wk. ACE2 KO mice were more susceptible than WT mice to HFD-mediated glycemic dysregulation. Islet ACE2 activity and expression of various genes, including ANG II type 1a receptor (mAT1aR) were then assessed. Surprisingly, we observed no change in islet ACE2 activity and expression despite local RAS overactivity, indicated by an upregulation of mAT1aR expression. Despite a predominant expression in islet α-cells, further investigation highlighted a minor role for ACE2 on glucagon expression. Further, pancreatic ACE2 gene therapy improved glycemia in HFD-fed WT mice, leading to enhanced glucose-stimulated insulin secretion, reduced pancreatic ANG II levels, fibrosis, and ADAM17 activity. Altogether, our study demonstrates that HFD feeding increases RAS activity and mediates glycemic dysregulation likely through loss of ACE2 present outside the islets but independently of changes in islet ACE2.

scholarly journals Leucine supplementation increases SIRT1 expression and prevents mitochondrial dysfunction and metabolic disorders in high-fat diet-induced obese mice

2012 ◽  
Vol 303 (10) ◽  
pp. E1234-E1244 ◽  
Author(s):  
Hongliang Li ◽  
Mingjiang Xu ◽  
Jiyeon Lee ◽  
Chaoyong He ◽  
Zhonglin Xie
Keyword(s):  
Insulin Resistance ◽  
Mitochondrial Dysfunction ◽  
High Fat Diet ◽  
Dominant Negative ◽  
Sirtuin 1 ◽  
Acid Oxidation ◽  
High Fat ◽  
Leucine Supplementation ◽  
Nicotinamide Phosphoribosyltransferase ◽  
Sirt1 Expression

Leucine supplementation has been shown to prevent high-fat diet (HFD)-induced obesity, hyperglycemia, and dyslipidemia in animal models, but the underlying mechanisms are not fully understood. Recent studies suggest that activation of Sirtuin 1 (SIRT1) is an important mechanism to maintain energy and metabolic homeostasis. We therefore examined the involvement of SIRT1 in leucine supplementation-prevented obesity and insulin resistance. To accomplish this goal, male C57BL/6J mice were fed normal diet or HFD, supplemented with or without leucine. After 2 mo of treatment, alterations in SIRT1 expression, insulin signaling, and energy metabolism were analyzed. Eight weeks of HFD induced obesity, fatty liver, mitochondrial dysfunction, hyperglycemia, and insulin resistance in mice. Addition of leucine to HFD correlated with increased expression of SIRT1 and NAMPT (nicotinamide phosphoribosyltransferase) as well as higher intracellular NAD+ levels, which decreased acetylation of peroxisome proliferator-activated receptor-γ coactivator 1α (PGC1α) and forkhead box O1 (FoxO1). The deacetylation of PGC1α may contribute to upregulation of genes controlling mitochondrial biogenesis and fatty acid oxidation, thereby improving mitochondrial function and preventing HFD-induced obesity in mice. Moreover, decreased acetylation of FoxO1 was accompanied by decreased expression of pseudokinase tribble 3 (TRB3) and reduced the association between TRB3 and Akt, which enhanced insulin sensitivity and improved glucose metabolism. Finally, transfection of dominant negative AMPK prevented activation of SIRT1 signaling in HFD-Leu mice. These data suggest that increased expression of SIRT1 after leucine supplementation may lead to reduced acetylation of PGC1α and FoxO1, which is associated with attenuation of HFD-induced mitochondrial dysfunction, insulin resistance, and obesity.

scholarly journals Allium-Derived Compound Propyl Propane Thiosulfonate (PTSO) Attenuates Metabolic Alterations in Mice Fed a High-Fat Diet through Its Anti-Inflammatory and Prebiotic Properties

Nutrients ◽  
2021 ◽  
Vol 13 (8) ◽  
pp. 2595
Author(s):  
Teresa Vezza ◽  
José Garrido-Mesa ◽  
Patricia Diez-Echave ◽  
Laura Hidalgo-García ◽  
Antonio J. Ruiz-Malagón ◽  
...  
Keyword(s):  
High Fat Diet ◽  
Immune Cell ◽  
Antimicrobial Properties ◽  
Organosulfur Compound ◽  
Experimental Models ◽  
High Fat ◽  
Metabolic Markers ◽  
Ppar Γ ◽  
Tnf Α ◽  
Different Doses

Background: Propyl propane thiosulfonate (PTSO) is an organosulfur compound from Allium spp. that has shown interesting antimicrobial properties and immunomodulatory effects in different experimental models. In this sense, our aim was to evaluate its effect on an experimental model of obesity, focusing on inflammatory and metabolic markers and the gut microbiota. Methods and results: Mice were fed a high-fat diet and orally treated with different doses of PTSO (0.1, 0.5 and 1 mg/kg/day) for 5 weeks. PTSO lessened the weight gain and improved the plasma markers associated with glucose and lipid metabolisms. PTSO also attenuated obesity-associated systemic inflammation, reducing the immune cell infiltration and, thus, the expression of pro-inflammatory cytokines in adipose and hepatic tissues (Il-1ẞ, Il-6, Tnf-α, Mcp-1, Jnk-1, Jnk-2, Leptin, Leptin R, Adiponectin, Ampk, Ppar-α, Ppar-γ, Glut-4 and Tlr-4) and improving the expression of different key elements for gut barrier integrity (Muc-2, Muc-3, Occludin, Zo-1 and Tff-3). Additionally, these effects were connected to a regulation of the gut microbiome, which was altered by the high-fat diet. Conclusion: Allium-derived PTSO can be considered a potential new tool for the treatment of metabolic syndrome.

scholarly journals Hypothalamic Microglial Heterogeneity and Signature under High Fat Diet–Induced Inflammation

2021 ◽  
Vol 22 (5) ◽  
pp. 2256
Author(s):  
Natália Ferreira Mendes ◽  
Carlos Poblete Jara ◽  
Ariane Maria Zanesco ◽  
Eliana Pereira de Araújo
Keyword(s):  
High Fat Diet ◽  
Ex Vivo ◽  
Experimental Models ◽  
High Fat ◽  
Inflammatory Stimuli ◽  
Hypothalamic Inflammation ◽  
Signaling Activation ◽  
New Research ◽  
Fat Feeding

Under high-fat feeding, the hypothalamus atypically undergoes pro-inflammatory signaling activation. Recent data from transcriptomic analysis of microglia from rodents and humans has allowed the identification of several microglial subpopulations throughout the brain. Numerous studies have clarified the roles of these cells in hypothalamic inflammation, but how each microglial subset plays its functions upon inflammatory stimuli remains unexplored. Fortunately, these data unveiling microglial heterogeneity have triggered the development of novel experimental models for studying the roles and characteristics of each microglial subtype. In this review, we explore microglial heterogeneity in the hypothalamus and their crosstalk with astrocytes under high fat diet–induced inflammation. We present novel currently available ex vivo and in vivo experimental models that can be useful when designing a new research project in this field of study. Last, we examine the transcriptomic data already published to identify how the hypothalamic microglial signature changes upon short-term and prolonged high-fat feeding.

scholarly journals Fast Induction of Hcc in Nash Rodent Model: A Simple Diet Associated with A Chemical Carcinogen

2020 ◽  
Vol 4 (2) ◽  
Keyword(s):  
High Fat Diet ◽  
Tumor Development ◽  
Immunohistochemical Analysis ◽  
Experimental Models ◽  
Rodent Model ◽  
New Drugs ◽  
Sprague Dawley ◽  
High Fat ◽  
Deficient Diet ◽  
Alcoholic Fatty Liver

Introduction: Non-alcoholic fatty liver disease (NAFLD) have been increasing as an important cause of hepatocellular carcinoma (HCC). Experimental models are crucial to identify some pathways in the pathogenesis of HCC secondary to NAFLD. Objective: To systematize an experimental hybrid rodent model of HCC secondary to NAFLD. Material and Methods: Fourteen male Sprague-Dawley rats, weighting 350-500g, were fed with choline-deficient high-fat diet and diethylnitrosamine (DEN) in the drinking water for 16 weeks. The animals were separated into two groups: 7 received DEN in water (100mg/ml) associated to choline-deficient high-fat diet and 7 received only cholinedeficient high-fat diet. Histological and immunohistochemical analysis were also performed. Results: All animals had definitive diagnosis of NASH in both groups with hepatocellular ballooning, steatosis and inflammation. In the group that received high-fat choline deficient diet, only two animals had micro nodular cirrhosis. However, in DEN group with high-fat choline deficient diet, all animals had gross lesions, major nodulations and fibrosis, visible in macroscopy. Besides, according of Edmondson-Steiner classification, 71% of the animals that received DEN + Diet with positive CK19 and oval cells and developed some grades of dysplastic and tumoral lesions. Moreover, in this model we could identify beyond NASH progression, some tumor-development stages, which means this model shows different treatment and study targets. Conclusion: The model is accomplishable, promotes fast induction of HCC in NAFLD context without much complexity to be executed and will be implemented as an interesting model to study new drugs to HCC secondary a NASH.

scholarly journals Dietary Lycium barbarum Polysaccharide Induces Nrf2/ARE Pathway and Ameliorates Insulin Resistance Induced by High-Fat via Activation of PI3K/AKT Signaling

2014 ◽  
Vol 2014 ◽  
pp. 1-10 ◽  
Author(s):  
Yi Yang ◽  
Wang Li ◽  
Yan Li ◽  
Qing Wang ◽  
Ling Gao ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
High Fat Diet ◽  
Glycogen Synthase ◽  
Akt Signaling ◽  
Experimental Models ◽  
Related Factor ◽  
High Fat ◽  
Lycium Barbarum

Lycium barbarum polysaccharide (LBP), an antioxidant from wolfberry, displays the antioxidative and anti-inflammatory effects on experimental models of insulin resistance in vivo. However, the effective mechanism of LBP on high-fat diet-induced insulin resistance is still unknown. The objective of the study was to investigate the mechanism involved in LBP-mediated phosphatidylinositol 3-kinase (PI3K)/AKT/Nrf2 axis against high-fat-induced insulin resistance. HepG2 cells were incubated with LBP for 12 hrs in the presence of palmitate. C57BL/6J mice were fed a high-fat diet supplemented with LBP for 24 weeks. We analyzed the expression of nuclear factor-E2-related factor 2 (Nrf2), Jun N-terminal kinases (JNK), and glycogen synthase kinase 3β (GSK3β) involved in insulin signaling pathway in vivo and in vitro. First, LBP significantly induced phosphorylation of Nrf2 through PI3K/AKT signaling. Second, LBP obviously increased detoxification and antioxidant enzymes expression and reduced reactive oxygen species (ROS) levels via PI3K/AKT/Nrf2 axis. Third, LBP also regulated phosphorylation levels of GSK3β and JNK through PI3K/AKT signaling. Finally, LBP significantly reversed glycolytic and gluconeogenic genes expression via the activation of Nrf2-mediated cytoprotective effects. In summary, LBP is novel antioxidant against insulin resistance induced by high-fat diet via activation of PI3K/AKT/Nrf2 pathway.

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